TY - JOUR
T1 - The protective effects of rutaecarpine on gastric mucosa injury in rats
AU - Wang, Li
AU - Hu, Chang Ping
AU - Deng, Pan Yue
AU - Shen, Shen Si
AU - Zhu, Hui Qing
AU - Ding, Jin Song
AU - Tan, Gui Shan
AU - Li, Yuan Jian
PY - 2005/5
Y1 - 2005/5
N2 - Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects gastric mucosa against injury induced by acetylsalicylic acid (ASA) and that rutaecarpine activates vanilloid receptors to evoke CGRP release. In the present study, we examined the protective effects of rutaecarpine on gastric mucosa injury, and explored whether the protective effects of rutaecarpine are related to stimulation of endogenous CGRP release via activating vanilloid receptors in rats. In an ASA-induced ulceration model, gastric mucosal ulcer index, pH value of gastric juice and plasma concentrations of CGRP were determined. ASA significantly increased the gastric mucosal ulcer index and the back-diffusion of H+ through the mucosa. Rutaecarpine at the doses of 100 or 300 μg/kg (i.v.), and 300 or 600 μg/kg (intragastric, i.g.) reduced the ulcer index and back-diffusion of H +, which was abolished by pretreatment with capsaicin (50 mg/kg, s.c.) or capsazepine (3 mg/kg, i.v.), a competitive vanilloid receptor antagonist. Rutaecarpine significantly increased the plasma concentration of CGRP, which was also abolished by capsazepine. In a stress-induced ulceration model, rutaecarpine reduced gastric mucosal damages, which was abolished by capsazepine (5 mg/ kg, i.p.). These results suggest that rutaecarpine protects the gastric mucosa against injury induced by ASA and stress, and that the gastroprotective effect of rutaecarpine is related to a stimulation of endogenous CGRP release via activation of the vanilloid receptor.
AB - Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects gastric mucosa against injury induced by acetylsalicylic acid (ASA) and that rutaecarpine activates vanilloid receptors to evoke CGRP release. In the present study, we examined the protective effects of rutaecarpine on gastric mucosa injury, and explored whether the protective effects of rutaecarpine are related to stimulation of endogenous CGRP release via activating vanilloid receptors in rats. In an ASA-induced ulceration model, gastric mucosal ulcer index, pH value of gastric juice and plasma concentrations of CGRP were determined. ASA significantly increased the gastric mucosal ulcer index and the back-diffusion of H+ through the mucosa. Rutaecarpine at the doses of 100 or 300 μg/kg (i.v.), and 300 or 600 μg/kg (intragastric, i.g.) reduced the ulcer index and back-diffusion of H +, which was abolished by pretreatment with capsaicin (50 mg/kg, s.c.) or capsazepine (3 mg/kg, i.v.), a competitive vanilloid receptor antagonist. Rutaecarpine significantly increased the plasma concentration of CGRP, which was also abolished by capsazepine. In a stress-induced ulceration model, rutaecarpine reduced gastric mucosal damages, which was abolished by capsazepine (5 mg/ kg, i.p.). These results suggest that rutaecarpine protects the gastric mucosa against injury induced by ASA and stress, and that the gastroprotective effect of rutaecarpine is related to a stimulation of endogenous CGRP release via activation of the vanilloid receptor.
KW - Calcitonin gene-related peptide
KW - Gastric acid
KW - Gastric mucosal ulcer index
KW - Rutaecarpine
KW - Vanilloid receptors
UR - http://www.scopus.com/inward/record.url?scp=20544451368&partnerID=8YFLogxK
U2 - 10.1055/s-2005-864135
DO - 10.1055/s-2005-864135
M3 - Article
C2 - 15931578
AN - SCOPUS:20544451368
SN - 0032-0943
VL - 71
SP - 416
EP - 419
JO - Planta Medica
JF - Planta Medica
IS - 5
ER -